Intimate associations exist between atherosclerosis and inflammation. The atherosclerotic process itself has[unreadable] features of chronic inflammation. Furthermore, the process of atherosclerosis is profoundly accelerated by[unreadable] chronic inflammatory disease states such as rheumatoid arthritis. Recently higher rates of first and[unreadable] subsequent myocardial infarctions, as well as strokes, were observed in patients with acute urinary and[unreadable] respiratory infections. Perhaps most notable amongst the plethora of metabolic changes that affect lipid and[unreadable] lipoproteins during inflammation are the structural and metabolic alterations of HDL. In practically all species[unreadable] there is a significant decrease of HDL cholesterol and apolipoprotein A-l (apoA-l). Serum amyloid A protein[unreadable] (SAA) is dramatically induced by cytokines and can even become the major apolipoprotein of HDL. The[unreadable] same cytokines concomitantly induce the inflammatory phospholipases particularly group MA secretory[unreadable] phospholipase A2 (group IIA sPLA2) that hydrolyze HDL surface phospholipids with significant metabolic[unreadable] sequelae. In the short term these changes are likely required for survival, but if chronically maintained could[unreadable] have long-term pathological consequences.[unreadable] The thesis of this proposal is that the acute phase phospholipases (group IIA sPLA2) act in concert[unreadable] with cholesterol ester transfer protein (CETP) to propel the apolipoproteins (SAA and apoA-l)[unreadable] associated with spherical HDL to distinct lipid-poor SAA or apoA-l entities (including prep HDL)[unreadable] and/or even "free" apolipoproteins. This process hold major implications for HDL function and[unreadable] metabolism during inflammation. Specifically, the lipid-poor apoA-l and SAA entities likely promote[unreadable] cholesterol efflux whilst at the same time being susceptible to accelerated catabolism.